GI: Part 1 Flashcards
Large Intestine
Micro-organisms in the colon break down proteins left over from the small intestine. Amino acids are deaminated by the bacteria, leaving AMMONIA (Hepatic encepholapthy/altered mental status), which is then converted to UREA in the liver.
Liver
Carbohydrate metabolism
Glycogenesis, glycogenolysis, gluconeogenesis
Protein metabolism
Synthesis of nonessential amino acids, synthesis of plasma proteins, urea formation from NH3
Also synthesizes albumins, globulins, fibrinogens, and other proteins involved in clotting
Liver: Bilirubin
Bilirubin Metabolism:
Bilirubin is a pigment derived from the breakdown of red blood cells. Constantly being produced by the body.
It is insoluble in water so it is bound to albumin and transported to the liver. This is UNCONJUGATED bilirubin (Indirect Bilirubin)
Normal = 0-14 (p. 883, table 39.6)
In the liver, bilirubin combines with glucuronic acid and becomes soluble in water. This is CONJUGATED bilirubin (Direct Bilirubin) Normal = 0-5.1
Urea breath test
Urea breath test—rapid diagnostic test for Helicobacter Pylori. Based on the ability of H. Pylori to convert urea to ammonia. Patient inhales urea laced with radioisotopes. Exhaled breath analyzed. H.Pylori cause of peptic ulcers
Treat H pylori with 2 antibiotics, 1 PPI
Liver Biopsy
Used to obtain sample of hepatic tissue—analyzed for cancer, cirrhosis and fibrosis
Open Liver Biopsy—incision made and wedge of tissue removed.
Closed Liver Biopsy-percutaneous procedure. Patient lies in supine position with right arm above head. Needle inserted between 6th and 9th intercostal spaces on the right.
***Major complication—-BLEEDING. Patient is on bedrest for at least 6 hours post-procedure and lies on right side for first few hours to put pressure on the insertion point and minimize risk of hemorrhage.
Upper GI bleeding
Common causes:
Peptic ulcer disease
Primary factor is H. pylori, ingestion of ASA, NSAIDs, corticosteroids, smoking
Stress-related erosive syndrome
Decreased perfusion of stomach mucosa, related to physiological stress (decreased splanchnic perfusion)
Esophageal varices
Collateral circulation as a result of portal hypertension, rising pressure causes tortuous distended veins or varices
Peptic Ulcer Disease
Erosion of the GI mucosa resulting from the digestive action of HCL acid and Pepsin. ***H. Pylori present in more than 75% cases of gastric ulcers and 90% duodenal ulcers.
More common in women and those of low socioeconomic status.
***Increased incidence for smokers (nicotine promotes reflux of duodenal contents into the stomach), alcoholics, and those who take NSAIDs or ASA frequently.
Ulcers can perforate—require emergency treatment.
Upper GI Bleed
Mallory-Weiss tears
Laceration of the distal esophagus, gastroesophageal junction, and cardia of the stomach
Heavy alcohol use, binge drinking, forceful vomiting/retching, or violent coughing.
Dieulafoy’s lesions
Vascular malformations, usually in the proximal stomach
Upper GI Bleeding: Clinical Presentation
Orthostatic hypotension: increase in pulse > 20 bpm and drop in BP < 10 mmHg below baseline from sitting to standing Cool, clammy skin Hematemesis Hematochezia: blood in stool Melena: tarry black stool Coffee-ground emesis: blood with HCl upper GI bleed HIGH BUN: from hypovolemia Hypokalemia/Metabolic alkalosis
Lab Work for Upper GI Bleed
Decreased H& H
Mild leukocytosis & hyperglycemia (response to stress)
Increase BUN (large protein load from breakdown of Hgb)
Hypernatremia (result of emesis)
Hypokalemia (result of emesis)
Prolonged PT/PTT (liver dysfunction or use of anticoagulation?)
Thrombocytopenia (cirrhosis & portal HTN with splenomegaly)
Hypoxemia (decreased Hgb impairing O2 carrying capacity)
Classic Symptoms of GI Bleeding
Hematemesis
Indicates bleeding above the ligament of Trietz (suspensory muscle that connects duodenum to diaphragm)
Bright red indicates
active, profuse bleeding
“Coffee-ground” emesis is
RBCs broken down with HCL acid, causing it to turn brown
Classic Symptoms of GI Bleeding: Hematochezia
This is the passage of fresh blood through the anus, usually in or with stools.
Sometimes written as “BRBPR” Bright Red Blood Per Rectum
**Hematochezia is commonly associated with **lower GI bleeding, but may also occur from a brisk upper gastrointestinal bleed.
Classic Symptoms of GI Bleeding: Melena
Melena
Blood in the stools that turns them black (tarry) and foul smelling. The black color is caused by oxidation of the iron in hemoglobin during its passage through the ileum and colon
- **Indicates upper GI bleeding in 90% of cases
- **May take several days to clear stools
- **Stools will remain positive for occult blood for 1 to 2 weeks (detected by positive guaiac test)
Esophageal Varices:
Usually form as a result of liver cirrhosis. Complex of tortuous veins at the lower end of the esophagus. Swollen and engorged due to portal hypertension. Varices contain little elastic tissue and are quite fragile. May rupture as a result of coughing, sneezing, vomiting etc.
Management of UGI Bleeds
Two large-bore IVs or rapid central line insertion
Fluids- isotonic (normal saline)
Blood products (T&C for 4 units of PRBC stat). Calcium may drop, but it’s normal.
Fluids: LR or NS. May need CVP line or PA catheter to monitor effectiveness and avoid overresuscitation
T&C early!
If large amts of PRBCs transfused: hypocalcemia may result from citrate in stored blood that binds to calcium. Calcium administration may be required
OXYGEN!! To support tissue perfusion—prevents ischemia & dysrythmias
Foley insertion to monitor I&O
Vitamin K and/or FFP and platelets if coagulopathic
Vasoactives may be needed until fluid volume re-established
